Drug interactions with lipid-lowering drugs: Mechanisms and clinical relevance¶
Neuvonen, Niemi, & Backman. (2006). Drug interactions with lipid-lowering drugs: Mechanisms and clinical relevance: Mechanisms and clinical relevance. Clinical Pharmacology & Therapeutics.
Cited by¶
2 citations across 2 artifacts.
Each citation links to the sentence it supports in the citing article.
Domain-specific¶
- Metabolic Inactivation
- Simvastatin, a widely prescribed cholesterol-lowering statin given as a lactone prodrug, is metabolised primarily by hepatic CYP3A4
This sourceThe CYP3A4-dependent metabolism of simvastatin (its acid also via CYP2C8) and the resulting sensitivity of its plasma levels to CYP3A4 inhibitors. How interaction-driven rises in statin plasma concentrations increase the risk of myopathy and rhabdomyolysis.
Supported in partVerified against the source
- Simvastatin, a widely prescribed cholesterol-lowering statin given as a lactone prodrug, is metabolised primarily by hepatic CYP3A4
- Polypharmacy
- For pharmacokinetic risk, the analyst scans for shared elimination pathways — two CYP3A4 substrates, or an inhibitor added to an existing substrate — and infers an exposure-multiplying collision (a calcium-channel blocker inhibiting CYP3A4 raises statin levels and myopathy risk
This sourceNeuvonen and colleagues' review of CYP3A4-dependent statins whose plasma concentrations and myotoxicity risk are greatly increased by strong CYP3A4 inhibitors, with verapamil and diltiazem named as weak or moderately potent inhibitors usable cautiously at small statin doses.
Supported in partVerified against the publisher's abstract
“Simvastatin, lovastatin, and atorvastatin are metabolized by cytochrome P450 (CYP) 3A4”
- For pharmacokinetic risk, the analyst scans for shared elimination pathways — two CYP3A4 substrates, or an inhibitor added to an existing substrate — and infers an exposure-multiplying collision (a calcium-channel blocker inhibiting CYP3A4 raises statin levels and myopathy risk
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